Evidence map›Paper›PMID 27376578›Full record

ArticleNature medicine2016

p53 induces formation of NEAT1 lncRNA-containing paraspeckles that modulate replication stress response and chemosensitivity.

Carmen Adriaens, Laura Standaert, Jasmine Barra, Mathilde Latil, Annelien Verfaillie, Peter Kalev, Bram Boeckx, Paul W G Wijnhoven, Enrico Radaelli, William Vermi and 11 more

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Nature medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 310 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
310citing papers in PubMed, 1 pooled it
21.3field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

310 citing papers in PubMed, 1 synthesis or guideline pooled it, 467 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Intercellular transfer of LncRNABiochemistry and biophysics reports · 2026
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  5. Review
  6. Article
  7. Review
  8. The Role of Long Noncoding RNAs in Modulation of Stress Granules in Cancer.Journal of cellular and molecular medicine · 2026
    Review
  9. iScience · 2026
    Article
  10. The Polymers of Life: Exploring Cellular Function Through Polymer Concepts.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  11. Review
  12. Article
  13. Review
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  15. Article
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  18. Article
  19. Article
  20. Article

250 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 8 institutions in 5 countries.

Carmen AdriaensLaboratory for Molecular Cancer Biology, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.
Laura StandaertLaboratory for Molecular Cancer Biology, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.
Jasmine BarraLaboratory for Molecular Cancer Biology, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.
Mathilde LatilUniversité Libre de Bruxelles, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Bruxelles, Belgium.
Annelien VerfaillieLaboratory of Computational Biology, Center for Human Genetics, KU Leuven, Leuven, Belgium.
Peter KalevLaboratory for Mechanisms of Cell Transformation, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.
Bram BoeckxVesalius Research Center, VIB, KU Leuven, Leuven, Belgium.
Paul W G WijnhovenThe Wellcome Trust/Cancer Research UK Gurdon Institute, University of Cambridge, Cambridge, UK.
Enrico RadaelliMouse Histopathology Core Facility, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.
William VermiSection of Pathology, Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy.
Eleonora LeucciLaboratory for Molecular Cancer Biology, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.ORCID 0000-0002-2898-748X
Gaëlle LapougeUniversité Libre de Bruxelles, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Bruxelles, Belgium.
Benjamin BeckUniversité Libre de Bruxelles, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Bruxelles, Belgium.
Joost van den OordLaboratory of Translational Cell and Tissue Research, Department of Pathology, KU Leuven and UZ Leuven, Leuven, Belgium.
Shinichi NakagawaRNA Biology Laboratory, RIKEN, Wako, Japan.
Tetsuro HiroseInstitute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
Anna A SablinaLaboratory for Mechanisms of Cell Transformation, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.
Diether LambrechtsVesalius Research Center, VIB, KU Leuven, Leuven, Belgium.
Stein AertsLaboratory of Computational Biology, Center for Human Genetics, KU Leuven, Leuven, Belgium.
Cédric BlanpainUniversité Libre de Bruxelles, Institut de Recherche Interdisciplinaire en Biologie Humaine et Moléculaire, Bruxelles, Belgium.
Jean-Christophe MarineLaboratory for Molecular Cancer Biology, Center for the Biology of Disease, VIB, KU Leuven, Leuven, Belgium.
VIB-KU Leuven Center for Cancer Biology · BEUniversité Libre de Bruxelles · BEHokkaido University · JPKU Leuven · BEVIB-KU Leuven Center for Microbiology · BEUniversitair Ziekenhuis Leuven · BEUniversity of Cambridge · GBWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In a search for mediators of the p53 tumor suppressor pathway, which induces pleiotropic and often antagonistic cellular responses, we identified the long noncoding RNA (lncRNA) NEAT1. NEAT1 is an essential architectural component of paraspeckle nuclear bodies, whose pathophysiological relevance remains unclear. Activation of p53, pharmacologically or by oncogene-induced replication stress, stimulated the formation of paraspeckles in mouse and human cells. Silencing Neat1 expression in mice, which prevents paraspeckle formation, sensitized preneoplastic cells to DNA-damage-induced cell death and impaired skin tumorigenesis. We provide mechanistic evidence that NEAT1 promotes ATR signaling in response to replication stress and is thereby engaged in a negative feedback loop that attenuates oncogene-dependent activation of p53. NEAT1 targeting in established human cancer cell lines induced synthetic lethality with genotoxic chemotherapeutics, including PARP inhibitors, and nongenotoxic activation of p53. This study establishes a key genetic link between NEAT1 paraspeckles, p53 biology and tumorigenesis and identifies NEAT1 as a promising target to enhance sensitivity of cancer cells to both chemotherapy and p53 reactivation therapy.

Indexed as

AnimalsAtaxia Telangiectasia Mutated ProteinsCarcinogenesisCell Line, TumorDNA DamageFlow CytometryGene Expression Regulation, NeoplasticHumansImmunoblottingImmunohistochemistryIn Situ Hybridization, FluorescenceKaplan-Meier EstimateMCF-7 CellsMicePoly(ADP-ribose) Polymerase InhibitorsPrecancerous ConditionsAtaxia Telangiectasia Mutated ProteinsAtr protein, mouseNEAT1 long non-coding RNA, humanNEAT1 long non-coding RNA, mousePoly(ADP-ribose) Polymerase InhibitorsRNA, Long NoncodingTumor Suppressor Protein p53

Identifiers

PMID27376578
OpenAlexW2473225834

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.